Interferon-alphabeta mediates partial control of early pulmonary Mycobacterium bovis bacillus Calmette-Guérin infection.

Kuchtey J, Fulton SA, Reba SM, Harding CV, Boom WH
Immunology. 2006 118 (1): 39-49

PMID: 16630021 · PMCID: PMC1782276 · DOI:10.1111/j.1365-2567.2006.02337.x

The role of type I interferon (IFN-alphabeta) in modulating innate or adaptive immune responses against mycobacterial infection in the lung is unclear. In this study we investigated the susceptibility of IFN-alphabeta-receptor-deficient (IFN-alphabetaR-/-) mice to pulmonary infection with aerosolized Mycobacterium bovis bacillus Calmette-Guérin (BCG). During early infection (2-3 weeks), enhanced growth of BCG was measured in the lungs of IFN-alphabetaR-/- mice compared to wild-type mice. However, during late infection the burden of BCG was similar in the lungs of IFN-alphabetaR-/- and wild-type mice. Although control of BCG growth was delayed, recruitment and activation of T and natural killer cells, production of IFN-gamma, and cytokine expression were all similar in wild-type and IFN-alphabetaR-/- mice. However, decreased expression of nitric oxide in bronchoalveolar lavage fluids from IFN-alphabetaR-/- mice correlated with enhanced growth of BCG. Bone marrow-derived macrophages from IFN-alphabetaR-/- mice also produced less nitric oxide following infection with BCG in vitro. These findings suggest that IFN-alphabeta contributes to innate immunity to pulmonary mycobacterial infection by augmenting production of nitric oxide.

MeSH Terms (20)

Animals Bronchoalveolar Lavage Fluid Cells, Cultured Female Immunity, Innate Interferon-gamma Killer Cells, Natural Lung Lymphocyte Activation Macrophages Male Membrane Proteins Mice Mice, Knockout Mycobacterium bovis Nitric Oxide Receptor, Interferon alpha-beta Receptors, Interferon T-Lymphocyte Subsets Tuberculosis, Pulmonary

Connections (1)

This publication is referenced by other Labnodes entities: